CAMK2g ELISA kit
- Known as:
- CAMK2g Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CAMK2g-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CAMK2g ELISA kit
Related genes to: CAMK2g ELISA kit
- Gene:
- CAMK2G NIH gene
- Name:
- calcium/calmodulin dependent protein kinase II gamma
- Previous symbol:
- CAMKG
- Synonyms:
- -
- Chromosome:
- 10q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2016-10-05
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- The progressive lung function decline in severe asthma is poorly explained by traditional inflammation‑centered paradigms. Calcium (Ca²⁺) dysregulation and transforming growth factor‑β (TGF‑β) signaling have been implicated, but the molecular link between them and their upstream regulators remain elusive. - Source: PubMed
Publication date: 2026/08/14
Zhu ZhiqinXiao QingaoCai RunjinQi EnyuGong XiaoxiaoTang JialeLi XiaozhaoFeng Juntao - Osteoporosis features excessive osteoclast-mediated bone resorption, and long-term safety concerns with current antiresorptives and rebound after discontinuation underscore the need for new therapeutic targets. Calcium/calmodulin-dependent kinases (CaMKs) have been linked to osteoclastogenesis, yet which CaMKII isoform is functionally essential and therapeutically actionable remains incompletely defined. Here, we investigated the role of calcium/calmodulin-dependent protein kinase II gamma (CaMKIIγ) in the osteoclast lineage, examined its downstream signaling mechanisms, and evaluated whether its pharmacological inhibition protects against ovariectomy-induced bone loss. CaMKIIγ expression increased during osteoclastogenesis induced by receptor activator of NF-κB ligand (RANKL), and shRNA-mediated Camk2g knockdown in RAW 264.7 cells markedly reduced multinucleated osteoclast formation. Functionally, Camk2g knockdown disrupted F-actin ring organization and reduced osteoclast resorptive pit formation. Berbamine (BBM), a reported CaMKIIγ inhibitor, phenocopied these inhibitory effects at non-cytotoxic concentrations during osteoclast differentiation, with maximal inhibition when applied during early differentiation. RNA sequencing and quantitative PCR revealed coordinated repression of osteoclastogenic gene programs upon CaMKIIγ inhibition. Pathway enrichment analyses implicated NF-κB signaling, and western blotting confirmed that Camk2g knockdown and BBM preferentially attenuated early RANKL-induced p65 phosphorylation, accompanied by reduced downstream nuclear factor of activated T cells 1 (NFATc1) induction. In ovariectomized mice, BBM administration at 25 or 50 mg/kg per day by intraperitoneal injection partially preserved trabecular microarchitecture and reduced osteoclast presence, as shown by micro-CT and histological staining. These findings identify CaMKIIγ as a regulator of osteoclastogenesis and support CaMKIIγ inhibition as a potential strategy to prevent postmenopausal bone loss. - Source: PubMed
Publication date: 2026/08/08
Qiu YisenFang NingnanAn BangTeng GanghongLuo HongshengWang WeidongXu YiweiWang Xinjia - Early diagnosis of seronegative rheumatoid arthritis (SNRA) is often challenging due to lack of reliable serological markers. The aim of this study was to explore protein biomarkers of SNRA and identify their potential as therapeutic targets. - Source: PubMed
Publication date: 2026/07/15
Zhang PengLiang YoubangLi XinYang YihongLiang WeidongYao XuemingShen ZhengdongWen YuZhan ChenguangWu XiaodongKe PeifengMei LiyanGao KaixinDu HaifangChen XiuminZhao LidanWang MaojieHuang Runyue - Classic BCR::ABL1-negative myeloproliferative neoplasms (MPNs)-polycythaemia vera, essential thrombocythaemia, and primary myelofibrosis-are clonal haematopoietic stem cell disorders with marked heterogeneity in clinical phenotype, disease trajectory, and therapeutic response. Genomic stratification by driver and cooperating mutations only partially accounts for this variability, leaving gaps in predicting thrombotic risk, fibrotic progression, leukaemic transformation, and treatment benefit. Proteomics bridges this gap by providing function-proximal readouts of protein abundance, post-translational modifications, pathway activity, and intercellular signalling that genomics and transcriptomics cannot capture, positioning it as a theranostic platform in which the same molecular readouts simultaneously inform diagnostic stratification and therapeutic decision-making. We propose a five-stage translational framework spanning from discovery-scale mass spectrometry and affinity-based plasma profiling to targeted validation, multicentre standardisation, and machine learning-integrated clinical panels. Proteomic evidence is synthesised across the following four disease axes: clonal fitness in haematopoietic stem and progenitor cells; bone marrow microenvironmental remodelling and fibrosis; chronic inflammation and thrombosis; and leukaemic transformation. We further describe how phosphoproteomics reveals resistance mechanisms to JAK inhibitors, including AXL-MAPK bypass and PP2A-autophagy-mediated tolerance, and how protein-level biomarkers (BCL2-BCL-XL, RAS-ERK, CAMK2G, and ROCK1/2) can guide individualised therapeutic selection. Affinity-based platforms (Olink PEA and SomaScan) and spatially resolved technologies (CODEX and single-cell proteomics) complement discovery proteomics. At present, however, this evidence base is constrained by small and heterogeneous cohorts, limited cross-platform reproducibility, and a scarcity of independent external validation for candidate protein panels. Realising this vision will require multicentre standardisation, analytically validated panel assays, and prospective clinical studies that translate molecular findings into decision-grade tools for patients with MPNs. - Source: PubMed
Publication date: 2026/06/14
Zhang JingHan Yan-Qiu - Atherosclerosis (AS) is a widespread cardiovascular disorder that constitutes a major contributor to global morbidity and mortality, thereby imposing significant economic burdens on healthcare systems worldwide. Efferocytosis, the phagocytic removal of apoptotic cells, serves as a fundamental mechanism for maintaining tissue homeostasis during normal physiological function and for restoring equilibrium following pathological insults. - Source: PubMed
Publication date: 2026/05/26
Qian JintaoZhang JunhaoWang JiahuiXu SuyuYu LiKong ChuiyuZhou Qing